Ruggieri M R, Hanno P M, Samadzadeh S, Johnson E W, Levin R M
J Urol. 1986 Jul;136(1):132-5. doi: 10.1016/s0022-5347(17)44757-4.
While it is well established clinically that urinary tract infection in the presence of outflow obstruction may be associated with difficulty in eradicating bacteria, it is not clear whether this is secondary to the presence of residual urine volume or other local effects of the obstruction such as attenuation of the intrinsic antibacterial defense mechanisms of the mucosal surface. Experiments in our laboratory and others over the past several years have demonstrated that the primary antibacterial defense mechanism of the bladder is the antiadherence effect of the bladder surface mucin layer. Additional studies have shown that heparin can duplicate this antiadherence activity of bladder mucin. The present report demonstrates that one hour of overdistension or ischemia and one week of partial outlet obstruction cause a functional defect in the intrinsic antiadherence effect of the bladder mucosa as evidenced by increased bacterial adherence. This defect can be reversed by heparin exposure prior to bacterial challenge. These results indicate that partial outlet obstruction and its potential sequelae such as overdistension and, particularly, mucosal ischemia, have dramatic adverse effects on the intrinsic antiadherence defense mechanism of the bladder. These effects can be reversed by intravesical exposure to an exogenous anionic polyelectrolyte (heparin).
虽然临床上已充分证实，存在流出道梗阻时的尿路感染可能与细菌根除困难有关，但尚不清楚这是继发于残余尿量的存在，还是梗阻的其他局部影响，如黏膜表面固有抗菌防御机制的减弱。在过去几年中，我们实验室和其他实验室的实验表明，膀胱的主要抗菌防御机制是膀胱表面黏蛋白层的抗黏附作用。进一步的研究表明，肝素可以复制膀胱黏蛋白的这种抗黏附活性。本报告表明，一小时的过度扩张或缺血以及一周的部分出口梗阻会导致膀胱黏膜固有抗黏附作用出现功能缺陷，这可通过细菌黏附增加得到证明。在细菌攻击之前暴露于肝素可逆转这种缺陷。这些结果表明，部分出口梗阻及其潜在后果，如过度扩张，尤其是黏膜缺血，会对膀胱的固有抗黏附防御机制产生显著的不利影响。通过膀胱内暴露于外源性阴离子聚电解质（肝素），这些影响可以得到逆转。
